Endurance performance declines with age (Hawkins and Wiswell, 2003; Heath et al., 1981; Kaminsky et al., 2015; Lepers and Stapley, 2016; Tanaka and Seals, 2008; Valenzuela et al., 2020). Specifically, there is a curvilinear pattern of decline in peak endurance performance, with a modest decrease from the age of 35 to 50–60 years and more notable declines after the age of 60 (Tanaka and Seals, 2008). Among others, reductions in the maximal O₂ uptake ( V ˙ O_2max) appears to be one of the most important factors affecting endurance performance during aging, with a 5%–10% reduction per decade starting from the age of 30 (Hawkins and Wiswell, 2003; Heath et al., 1981; Kaminsky et al., 2015; Lepers and Stapley, 2016; Tanaka and Seals, 2008; Valenzuela et al., 2020).

V ˙ O_2max is considered the gold standard measurement of integrated cardio-pulmonary and muscle function, and it quantifies the maximal rate of adenosine triphosphate (ATP) regeneration required for sustained muscle contractions during endurance exercise. The generation of aerobic ATP is dependent on the delivery of O₂ to muscle cells and its subsequent utilization via mitochondrial respiration. As elucidated by the conflation of Fick’s Principle and Fick’s Law of Diffusion, O₂ flows from ambient air to the mitochondria by convection and diffusion, driven by pressure gradients against numerous resistances in series. The collective dynamics of these relationships establish the conceptual basis of the O₂ cascade from lungs to the muscle tissue and enable the identification of specific limitations to V ˙ O_2max. The age-related decline in V ˙ O_2max is mostly attributable to diminished cardiac output, consequent to a reduction in maximal heart rate and cardiac output (Tanaka et al., 2001), but a specific role can also be attributed to reductions in skeletal muscle mass and function (Fleg and Lakatta, 1988).

In the last few decades, the endurance performance of the world-class master athletes has improved more rapidly than that of their younger counterparts (Lepers and Stapley, 2016), despite the inevitable age-related performance decline (Tanaka and Seals, 2008). This trend is attributed to advances in training strategies, together with an increase in the number of master athletes competing in endurance events, but it is still debated what are the physiological determinants of the preserved endurance performance in some aged adults (Lanza et al., 2025; Marcinek and Ferrucci, 2025). Master athletes, defined as individuals older than ∼35 years who train and compete in organized competitive events, provide a unique model for studying how regular training can mitigate or delay age-related physiological decline, accounting for the confounding effect of reduced physical activity levels (Mckendry et al., 2018; Valenzuela et al., 2020). Notably, master athletes with an average age of 67 years can exhibit V ˙ O_2max values comparable to those of healthy adults 3 decades younger (Mckendry et al., 2018). This high exercise capacity lends further support to the hypothesis that a 5%–7% decline in V ˙ O_2max per decade is characteristic of master endurance athletes over the age of 45 (Pollock et al., 1997; Trappe et al., 2013).

In this case study, we examined the training characteristics, physiological profile and performance of a male endurance athlete who set the world record in a 50-km race in the 80+ age category in the 2025 Master Championship in Malaga (Spain). Moreover, to identify the O₂ cascade profile, we tested the limiting factors of V ˙ O_2max using non-invasive measurements such as transthoracic bioimpedance and near-infrared spectroscopy (NIRS) during maximal cycling exercise.

In this case study, we analyzed the performance and the physiological profile of an 81-year-old Spanish athlete who broke the 50-km world record for men over 80 years of age in May 2025, and currently holds first place in the marathon world championship in the 80+ age category (2024-2025). The superior endurance performance observed in this master athlete was primarily explained by a well-preserved V ˙ O_2max, combined with a high fractional utilization of V ˙ O_2max and an enhanced capacity for fat oxidation. When limiting factors to V ˙ O_2max were explored on the cycle-ergometer, we observed fairly normal age-related cardiac output but highly preserved muscle oxidative and diffusive capacity. The unique data collected in our octogenarian elite athlete illustrate how endurance training in the late phase of life can attenuate or delay physiological changes associated to aging, thereby contributing to the characterization of healthy aging phenotypes.

Although age-related performance decline is inevitable (Tanaka and Seals, 2008), largely due to reductions in V ˙ O_2max associated with diminished cardiac output (Tanaka et al., 2001) and decrease in skeletal muscle mass and function (Fleg and Lakatta, 1988), regular physical activity may serve as an effective countermeasure (Valenzuela et al., 2020), eliciting beneficial adaptations at both the cardiovascular level and within skeletal muscle. Indeed, structural, functional, and electrical cardiac remodeling resulting from the physical and metabolic load placed on the heart (Beaudry et al., 2016) as well as improvements in muscle mass and mitochondrial capacity follow exercise training (Grevendonk et al., 2021).

In this study we collected functional indexes of endurance performance in an octogenarian elite athlete. The incremental running test showed a very high cardiorespiratory fitness relative to his age, as indicated by a V ˙ O_2max of 52.8 mL kg^-1·min^-1, which is to the best of our knowledge the highest value reported for an individual older than 80 years (the previous value was 50 mL kg^-1·min^-1) (Karlsen et al., 2015). For comparison, untrained age-matched individuals present values ranging from 18 to 25 mL kg^-1·min^-1 (Trappe et al., 2013), and the V ˙ O_2max obtained is equivalent to the 70th percentile for healthy males in their 20–30s (Liguori et al., 2022). As expected, this value was 19% lower when the athlete exercised on the cycle ergometer (2.510 vs. 3.110 L min^-1 in cycling and running, respectively) in accordance with the smaller muscle mass involved in the activity and previous studies showing lower V ˙ O_2max values in cycling compared to running test (14%–18% range) on running athletes (Bouckaert et al., 1990; Fernhall and Kohrt, 1990; Moreira-da-Costa et al., 1989). However, cycling V ˙ O_2max was still significantly higher than the values reported for untrained subjects of the same age (Trappe et al., 2013). This might also have clinical implications, particularly given that a higher V ˙ O_2max has been linked to a lower mortality risk even at the most advanced ages (Kokkinos et al., 2022).

To test the central limiting factors of V ˙ O_2max, heart rate, stroke volume, and cardiac output were monitored during the maximal cycling exercise. The maximal heart rate was lower compared to that of young athletes (∼190 bpm at 25 years old), although higher than predicted for his age (112%) (Tanaka et al., 2001). This result is not surprising if we consider ageing-related adaptations in autonomic control of heart rate (Tanaka et al., 2001). The stroke volume (128 mL) was also lower compared to young individuals (Zhou et al., 2001), in line with the decrease in cardiac tissue stiffness with age (Lakatta and Levy, 2003). The combination of these two factors resulted in a maximal cardiac output of 15.3 L min^-1 (corresponding to 9.6 L min^-1·m^-2 when normalized for body surface area), a value comparable to those recorded by cardiac blood pool imaging and echocardiography technique in 65-year-old untrained males subjects (16.7 L min^-1) but lower than the one of trained master athletes (19.1 L min^-1) (Seals et al., 1994). Other authors found higher peak exercise stroke volume (200 mL) and cardiac output (22.2 L min^-1, 11.4 L min^-1·m^-2 normalized for body surface area) in the former marathon world-record holder aged 77 years old (Foulkes et al., 2024). The difference in cardiac function between our athlete and the one recruited by others in the previous report may be due to the transient interruption of exercise training that our athlete faced in the middle aged. Indeed, detraining may have affected cardiac stiffness and blood/plasma volume, limiting ventricular filling (Carrick-Ranson et al., 2023; Coyle et al., 1986; Foulkes et al., 2024).

However, in the present athlete the reduction found in cardiac function was well compensated by a high value of Hb concentration, which allows for a large maximal oxygen delivery (Q̇aO₂) (3.281 L min^-1), higher than age-matched untrained individuals (∼2.900 mL L^-1, (Capelli et al., 2025)).

Nevertheless, the unique endurance performance and the high values of V ˙ O_2max were associated with remarkable peripheral adaptations at the level of the skeletal muscle. Indeed, the arterial-venous O₂ difference calculated was 164 mL L^-1, corresponding to an O₂ extraction of 75%, and the muscle oxidative capacity, as estimated by the muscle V ˙ O₂ recovery rate constant (4.67 min^-1) by NIRS was even better than young endurance-trained individuals (Brizendine et al., 2013). Classically, aging is associated with a progressive decline in skeletal muscle mitochondrial content and function, contributing to metabolic dysfunction in older adults (Fleg and Lakatta, 1988). However, exercise training can largely negate these age-related effects, as trained older adults exhibit higher levels of oxidative phosphorylation proteins and a preserved mitochondrial network. Although this topic is still debated in literature (Lanza et al., 2025; Marcinek and Ferrucci, 2025), our results seem to support the thesis that preserved exercise training habits have beneficial effects on mitochondrial capacity in aging populations (Grevendonk et al., 2021; Hood et al., 2019).

To better understand physiological adaptations in the O₂ cascade from the lungs to the mitochondria, we utilized the collected parameters to reconstruct the Wagner diagram (Figure 5) through the Helsinki O₂ Pathway Tool (Rissanen et al., 2024). This approach has been recently used by Goulding to demonstrate the role muscle diffusive capacity in response to sprint interval training from data collected by Mandic et al. (Goulding, 2024; Mandić et al., 2023). In Figure 5 it is possible to appreciate the unique features of our athlete in comparison to young healthy subjects. Although the V ˙ O_2max was similar between our athletes and young population, it is interesting to note that the calculated value of whole-body diffusion capacity corresponded to 75.3 mL min^-1·mmHg^-1, demonstrating outstanding diffusion capacity, higher than young healthy subjects (i.e., range 55–70 mL min^-1·mmHg^-1, (Goulding, 2024; Mandić et al., 2023)). This result was supported by the Δk value close to zero (0.07 min^-1). Δk is a non-invasive approach applied at the level of the skeletal muscle that utilizes NIRS data to collect information about relative muscle O₂ diffusion resistance. More specifically, the m V ˙ O₂ recovery rate constant is measured in non-limiting (i.e., HIGH tissue saturation index ranges) and limiting O₂ availability (LOW conditions), and the change in the recovery rate is related to limitations to intramuscular O₂ flux (Pilotto et al., 2022; Villanova et al., 2025). Thus, our athlete showed large adaptations in both oxidative and O₂ diffusion capacity in the skeletal muscle. These data support recent calculations made on V ˙ O₂max values in subjects ranging from 30 to 85–90 years old where authors reported a progressive decrease in V ˙ O₂ with aging associated to relevant impairments in peripheral resistance to O₂ muscular utilization rather than to reductions in the maximal cardiovascular transport of oxygen (Capelli et al., 2025). In this work, there was no specific information about the training status of the subjects but in our athlete we can speculate the observed peripheral adaptations were determined by a large volume endurance training, together with some high-intensity interval training sessions, which can positively affect muscle mass, capillary adaptations, and mitochondrial function/content (Liu et al., 2022; Bishop et al., 2014).

The exceptional physiological characteristics observed during exhaustion were also accompanied by unique submaximal features. The lactate threshold occurred at a velocity of 10.5 km h^-1 (80% of Vpeak) and corresponded to 91% of V ˙ O_2max. Such elevated levels of relative intensity are consistent with the physiological profiles of elite master athletes over 70 years of age, where lactate thresholds approaching 93% of V ˙ O_2max have been observed (Robinson et al., 2019). This value was higher than that observed in trained, but not elite, male athletes over the age of 60 and 70, where the lactate threshold (LT) corresponded respectively to 76.8% and 73.5% of V ˙ O_2max (Wiswell et al., 2000). The relative intensity of LT is also significantly higher than the one observed in young trained athletes (26 years old, V ˙ O_2max 60.2 mL kg^-1·min^-1), which showed a velocity at LT of 65.2% of maximal aerobic speed (Cerezuela-Espejo et al., 2018), and in elderly untrained (72 years old), where LT corresponded to ∼60% of V ˙ O_2max (Takeshima et al., 1996). The elevated LT intensity observed in this athlete may be explained by his specific training regimen, which predominantly consists of high-volume exercise performed near LT intensity, with no inclusion of sessions targeting V ˙ O_2max intensities.

MFO corresponding to 0.55 g min^-1 in this master athlete is comparable to normative data found in young athletic population (0.60 g min^-1 for men) (Achten et al., 2003; Amaro-Gahete et al., 2019b). Furthermore, his Fat_max was found at 77% of V ˙ O_2max, a value considerably higher compared to younger individuals (∼50%) (Achten et al., 2003; Amaro-Gahete et al., 2019b). The pronounced fat oxidation capacity observed may be attributed to the elevated muscle oxidative capacity, reflecting mitochondrial adaptations in both function and content that are closely associated with enhanced mitochondrial fatty acid oxidation (Dandanell et al., 2018), or alternatively reflects metabolic remodeling associated with keto-adaptation (Noakes et al., 2023). The record-holder peripheral advantages can be attributed to his specific training characteristics.

Among the physiological factors influencing running performance, we also evaluated O₂ cost of exercise. The athlete’s running economy was lower than the typical values reported for elite younger males (39.9 mL kg^-1·min^-1 at 14 km h^-1) and to those observed in younger recreational runners (36.7 mL kg^-1·min^-1 at 10 km·h^-1) (Barnes and Kilding, 2015). This value contrasts the exemplary running economy value (179 mL kg^-1·km^-1 at 12 km h^-1) demonstrated by a 70-year-old male marathon world record holder master athlete (Van Hooren and Lepers, 2023). We do not have a clear hypothesis for these differences, but it should be noted that our athlete is 10-year older than the marathon world record holder, and this gap may have affected tendon stiffness (Karamanidis and Arampatzis, 2006; Mademli and Arampatzis, 2008), resulting in a significant negative impact on running economy. Moreover, our athlete reported an average running distance of 65 km wk^-1, with a maximum of 120 km wk^-1 in the specific phases. In comparison, the 70-year-old male master marathon world record holder routinely ran 135–140 km wk^-1 (Van Hooren and Lepers, 2023). Thus, the lower weekly distance could have led to smaller adaptations that enhanced running economy (Morgan et al., 1995). It is also important to note that the O₂ cost of running was measured in fresh condition while it would have been of interest to have information about the running economy along the different segments of the 50-km race to better describe the unique performance (Zanini et al., 2024; Scheer et al., 2018). However, the race monitoring data revealed a 10% decrease in running speed, which is more pronounced than the 5% decrease observed in 40-year-old ultradistance running athletes following a 60-km ultramarathon (Schena et al., 2014).

This study captures an informative snapshot of the athlete’s physiology close to the 50-km record. More specifically, the distance from the establishment of the new 50-km record and the tests was 2 weeks. This is the optimal timeframe for evaluating physiological characteristics in proximity to performance, while simultaneously avoiding the inclusion of detrimental acute effects associated with long-distance running. Thus, our results seem to support an outstanding physiological profile of our athlete.

Nevertheless, it should be considered that we did not have longitudinal data that allowed us to trace the developmental trajectory or identify factors that shaped the physiological adaptations underlying this performance. Moreover, in the present study we investigated the physiological determinants of V ˙ O_2max by dissecting some of the steps along the O₂ cascade and linked their specific adaptations to training. However, we cannot exclude that the present athlete had unique genomic markers related to endurance performance (Psatha et al., 2024). Thus, future studies should try to follow longitudinal approaches and focus their attention on the link between outstanding athletic performance and unique genetic profiling.

Additionally, the comparisons of physiological determinants between our athlete and data from the literature was used to help the readers in better understanding the excellence of this case report. This approach was strengthen using comparable experimental approach between the present study and previous literature (Cerezuela-Espejo et al., 2018; Jaén-Carrillo et al., 2025; Randell et al., 2017), as well as high reproducible and valid testing. However, there are differences between exercising in the laboratory setting and performing a race on the field. For example, running economy was evaluated on a 1% uphill treadmill slope to more accurately reflect the energy cost of outdoor running (Jones and Doust, 1996) but there is likely a significant difference in running economy when running on a trail vs. running the same speed on a treadmill (Sabater et al., 2023). Thus, future study should try to explore physiological limitations of performance by also collecting data during actual athletic performance.

Finally, the approach used in the present study to identify limiting factors of V ˙ O_2max and the O₂ cascade profile involved a thorough examination of each factor mainly based on non-invasive techniques and several assumptions regarding blood composition (SaO₂, PaO₂, pH and temperature) during maximal exercise. Furthermore, the Helsinki O₂ Pathway Tool was used to calculate whole-body oxygen delivery and diffusion capacity, which allowed an estimation of the average systemic capacity to move and diffuse oxygen from blood vessels to cell, but not the specific response of the lower limbs. The readers should be aware that these approaches have some limitations compared to the direct Fick’s approach or invasive cardiopulmonary testing. For example, in this study arterial O₂ delivery to the muscles was estimated using Hb concentration in the venous blood but several conditions, and especially endurance training, lead to plasma volume expansion and can result in hemodilution, manifesting as reduced hematocrit and hemoglobin concentration (Montero and Lundby, 2018). However, the high degree of consistency between whole-body measurements and specific vastus lateralis variables (i.e., muscle oxygen diffusion capacity, as well as similarity in arterio-venous O₂ extraction calculated using Fick’s Principles or NIRS-derived Δ[deoxy (Hb + Mb)]) support the physiological meaning of the present results.

This case report on the world-record holder for the 50-km running distance in the male 80+ age category revealed the highest V ˙ O_2max recorded so far in octogenarians. Although running economy is lower than elite athletes and comparable to those of recreational runners, his performance is driven by relatively high fat oxidation metabolism and exceptional oxygen fractional utilization. The latter is explained by extraordinary skeletal muscle adaptation such as high oxidative and diffusive capacity, demonstrating well-adapted factors at the last steps of the oxygen cascade. Thus, the present findings reinforce the concept that maintaining high exercise capacity in advanced age supports the preservation of V ˙ O_2max, a key predictor of all-cause mortality, drawing attention to specific adaptations at the level of the skeletal muscle.